Gentlemen!

In the previous discussion of allopsychic delusions of explanation we could not avoid the fact that a large proportion of chronic psychotic states, whether they be temporary or permanent, are accompanied by sensory deceptions, admittedly—in the former case—just insofar as they coincide with episodes of acute illness. In addition, sensory deceptions can persist, even in cases of residual chronic mental disturbance, sometimes permanently, sometimes temporarily, or only on certain occasions. This appears to contradict all our preconceptions that conscious activity has returned to normal in residual paranoid states, since it is notable that, for sensory deceptions, there is a clear disturbance of conscious activity. If it has not returned to normal, then we ask ourselves whether any definite signs of a more florid, evolving disease process remain, when chronic mental disorder is accompanied by sensory deceptions. Gentlemen! The very fact that this question is raised proves to you the difficulty that often confronts us in deciding between residual mental disorder and chronic psychoses.

We would do well to avoid answering, until I have introduced a hypothesis about language, which, on its own, in my view, can guide us to deeper understanding of the essence of all mental illnesses. Here I remind you of our first patient, the gardener Rother who, incidentally, also suffers from sensory deceptions, albeit rarely and then only temporarily. How is it possible, we wonder, that in the same head such a vast quantity of misconceptions and misjudgments can exist side by side, in such contrast both among themselves and with reality, with well-preserved formal logic, apparent prudence, and totally accurate appreciation of the reality of his situation? Well, gentlemen, compared with the indisputable facts seen after the origin of his current condition, the answer is undeniable: It was the acute mental illness that created the gap in the solid structure of his associations. We will give this process of detachment an appropriate name and call it ‘sejunction’ [W]; we cannot fail to see it as a deficit, a break in continuity, which must correspond with failure of certain lines of association. The fact that, in the brain, different ideas and idea complexes are not merely juxtaposed, but are normally combined into larger groups, and finally into unity of the ego, can, in the final analysis, be due only to associative processes. The very fact that this patient is unaware of contradictions between his various misconceptions suggests that the combination of all higher associations into a single unit, the ego, has ceased. This individual consists simultaneously, as it were, of a number of different personalities: We could boldly call his condition a ‘disintegration of individuality’ [W]. It is perhaps just coincidence that this is so little evident in his outer appearance, because of the small demands made on his whole personality by his occupation. A gardener’s monotonous work is similar in this respect to that of an agricultural labourer, many factory workers, and even busy people whose work is single-mindedly manual, conforming to definite patterns. If it were a profession requiring development of a highly complex personality, such as a judge, a doctor, or an industrialist, disintegration of the personality would be revealed all the time in such occupations.

Gentlemen! We will see later that most signs of disturbed secondary identification, which make up symptoms of acute mental illness, can be explained by assuming the same sejunction process. Changes in content of consciousness, remaining as consequences of errors in identification, can therefore be traced back to sejunction.

Nevertheless, we also know that, other than healing, or persistence of changed content, there is a third way in which acute mental illness can develop: to varying degrees of dementia or feeble-mindedness. We can also derive dementia from the sejunction process, as we shall see later, because according to this, we define it just as a failure—or reduction—in associative activity.

With acute mental illnesses, you can often observe a shorter or longer stage, where, after a period of acute illness, a state somewhat similar in form may be present, albeit with changes in content, or with reduction in processes of active association, before a definitive return to full health. This stage of acute mental illness, whether paranoid or demented, is therefore still accessible to restitution.

All such considerations compel us to see in the sejunction process the real nature of acute mental illness. As the Rother example teaches us, prior episodes of sejunction can be readily seen in many old cases. In other cases, unmistakable progressive changes in content suggest the same chronic progression, albeit less obvious. Whether the disease eventually merges into a state of deficit, namely dementia, depends on the extent of the sejunction.

Gentlemen! We thus see that the sejunction hypothesis provides us with a key to understanding the most important phenomena of such conditions, which we can equate with deficit symptoms of brain diseases, equally for chronic as well as for acute mental disorders. However, a number of other symptoms appear to have no explanation in such terms, by which I mean ones we have regarded as ‘irritant’ symptoms, such as hallucinations. The better researched pathology of organic brain diseases gives us no explanation here, because the origins of even the most common symptoms of irritation—localized spasms and contractions—are still totally unknown to us. We learn only a little here from brain diseases: that these irritant symptoms are almost invariably linked to neurological deficits, and only from the latter do the former gain their clinical status. In some way, therefore, we should assume a causal relationship between deficit symptoms and irritation symptoms. But in our case, gentlemen, it is different, insofar as some irritant symptoms, such as hallucinations, are the most important symptoms of mental illness, apparently often occurring on their own. Should we not try to find some relationship to deficit symptoms, as an example of sejunction? This requirement is virtually forced on us by our clinical experiences, because we know of some mental illnesses which offer almost exclusively—throughout their entire course—only such irritant symptoms, and yet result in the same fateful outcomes, either falsification of content or dementia. As irritant symptoms are extinguished, deficits, whose full extent was hitherto unsuspected, then become apparent. With all due caution, you can at least say that the process of sejunction is accompanied by irritant symptoms, and may be obscured by them. It is entirely within the current framework of our ideas of disease processes that destroy nerves that they simultaneously act on nerves as a stimulus: The current theory of stimulation is indeed based on this. The same view probably prevails for ganglion cells. The time course of processes leading to death of nerves would then be a critical determinant of the occurrence of irritant effects. But perhaps also a purely mechanical concept of irritation, both plausible and comprehensible, is possible: As you will recall, we have taken mental activity to be a form of movement, which progresses in a closed chain of association sAZm in our schema. Memory images were, for us, sites of stored energy, always being refreshed from the ascending pathways, which access projection fields. This energy is being continually drained away, we may suppose, as charge on the projection field m declines, in readiness for their being called into action. Such continuous balancing up of energy can be inferred from the so-called unconscious mental activity, and from the circumstance that you always wake up from sleep with thoughts running through your head. According to general principles of mechanics, you would expect that disruption of such a flow of energy by sejunction would result in a build-up of energy, and thus localized enhancement of excitatory processes. Were this ‘nerve stream’ [W] to be readily comparable with fluid movement, you could then speak of a reflected wave in the nerve stream; but even without this, you might expect in ganglion cells—the main sites of stored-up energy—that voltage would increase, when run-off is impaired, but with continuation of influx, and this can easily overcharge the psychophysical movement to reach a wave peak (p. 46). In this sense it is probably not too bold to speak of ‘accumulated nervous energy’ [Ed]. Then the location of the sejunction process would be a critical determinant of any resulting irritant symptoms. Occurrence of hallucinations would suggest that sejunction on pathways sA would occur in a relatively confined range of pathways, or at least in one of the sensory projection fields, for example in an area of their output representations A.